Evidence map›Paper›PMID 35808996›Full record

ArticleThe clinical respiratory journal2022

Identification of genetic variants of the IL-22 gene in association with an altered risk of COPD susceptibility.

Yan Wang, Qipeng Zhou, Lingzhu Chen, Lian Dong, Mingmei Xiong, Xiaohui Xie, Li Zhao, Jingyi Xu, Zeguang Zheng, Jian Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in The clinical respiratory journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Yan WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Qipeng ZhouState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Lingzhu ChenState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Lian DongState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Mingmei XiongState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Xiaohui XieState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Li ZhaoState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Jingyi XuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Zeguang ZhengState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Jian WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Wenju LuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
First Affiliated Hospital of Guangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CNGuangzhou Medical University · CN

Funding

Guangxi Natural Science Foundation 2021GXNSFBA220064Guangzhou Department of Education 1201620007Guangzhou Science and Technology Program 202102010344Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program 2017BT01S155National Key R&D Program of China 2016YFC0903700National Natural Science Foundation of China 81220108001National Natural Science Foundation of China 81520108001National Natural Science Foundation of China 81770043National Natural Science Foundation of China 81800072National Natural Science Foundation of China 81900031Research Projects of SKLRD OP-201808Research Projects of SKLRD OP-201912Research Projects of SKLRD QN-201706Research Projects of SKLRD QN-201916Research Projects of SKLRD QN-201917
6 · The paper itself

Abstract

The incidence of chronic obstructive pulmonary disease (COPD) is related to the interaction between environmental exposure and genetic factors. Far more than 15% of smokers eventually develop COPD. In addition to smoking, genetic susceptibility may be another factor in the development of COPD. IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis. Here, we conducted a case-control study to evaluate the association between IL-22 tag-single nucleotide polymorphisms (SNPs) and COPD risk. Four tag-SNPs (rs2227478, rs2227481, rs2227484 and rs2227485) were identified according to linkage disequilibrium (LD) analysis in 30 healthy controls. A total of 513 COPD cases and 504 controls were recruited to perform an association study between these four tag-SNPs and COPD risk. We found that the "C" allele of rs2227478T>C and the "T" allele of rs2227481C>T were obviously related to decreased COPD susceptibility. Genetic model analysis showed that rs2227478T>C and rs2227481C>T were significantly associated with a decreased risk of COPD under dominant models after adjusting for the above factors. In the recessive model, rs2227485T>C was obviously associated with decreased COPD risk. Our data showed that only rs2227485T>C was associated with a decreased COPD risk after Bonferroni correction. The eQTL analysis showed that rs2227485T>C was significantly associated with IL-22 expression. The pGL4-rs2227485-C gene reporter had a higher promoter activity than pGL4-rs2227485-T. In our study, rs2227485T>C, located in the promoter region of IL-22, was associated with a decreased risk of COPD and increased IL-22 promoter activity, suggesting that this variant might modulate COPD susceptibility.

Indexed as

Pulmonary Disease, Chronic ObstructiveCase-Control StudiesGenetic Predisposition to DiseaseGenotypeHumansInterleukin-22InterleukinsPolymorphism, Single NucleotideInterleukin-22InterleukinsCOPDIL22promoter region activitySNP

Identifiers

PMID35808996
PMCPMC9376143
OpenAlexW4284988279

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.